The present invention relates to a method for controlling the subjective symptoms and objective signs of heart failure.
Heart failure, the consequence of various types of heart disease, is one of the most common and serious disorders affecting individuals of all ages. It is the pathophysiological state in which the heart is not able to pump blood at a rate commensurate with the requirement of body tissues. Abnormality of cardiac function, frequently but not always caused by a defect in myocardial contraction, leads to a short supply with blood from the heart.
During the last few decades, increased knowledge of the physiological and biochemical mechanism in cardiac contraction has provided precise definition of heart failure state. Unfortunately, for many decades, there were few advances in treatment of heart failure, with treatments generally limited to restriction of physical activity and sodium intake, and administration of digitalis and diuretics as well as vasodilators, non-glycosides inotropic agents and metabolism-improving agents. Digitalis glycosides, which have been available for nearly 200 years, increase the force of contraction in both normal and failing heart muscle. However, they have a narrow therapeutic range, and dosages are commonly limited by the toxic side effect. Catecholamines exert a positive inotropic effect by activating cardiac .beta..sub.1 -receptors, but their usefulness is limited by their arrhythmogenic properties, short duration of action and a general requirement for parenteral administration. Other inotropic agents, such as glucagon, theophilline and imidazole have not been accepted for general clinical application in the treatment of heart failure. Furthermore, there are some patients who cannot be controlled by digitalis glycosides, even in combined use with other usual treatment modalities for heart failure.
Thus, there is a need for a new method for treating heart failure.
Taurine(2-aminoethanesulfonic acid), a non-toxic amino acid, has been shown to exert positive inotropic activity in guinea pigs (Dietrich, J & Diacono: Life Sci., 10: 499, 1971). Also shown is an increase in taurine levels in the left ventricles of patients dying of chronic congestive heart failure (Huxtable, R & Bressler, R: Science, 184: 1187, 1974). Taurine is a normal constituent of the human diet and usually taken about 50 to 150 mg per day per person. However, there previously has been no attempt to administer large doses of taurine for the treatment of heart failure.